Of course they're true cells, and the fact that they don't reproduce
is nothing unusual.  Most cells don't reproduce.

  I think you've got to review the Cori cycle to understand how
anaerobic metabolism in muscle and red blood cells relies on the
*liver's* ability to oxidize lactate into pyruvate, and look more
closely into how cancer interferes with apoptosis.  Here's a passage
from /MBOC4/ p1010 on how important and normal apoptosis is:

-----
Programmed cell death (apoptosis)

The cells of a multicellular organism are members of a highly organized
community. The number of cells in this community is tightly regulated -
not simply by controlling the rate of cell division, but also by
controlling the rate of cell death. If cells are no longer needed, they
commit suicide by activating an intracellular death program. This
process is therefore called *programmed cell death,* although it is more
commonly called *apoptosis* (from a Greek word meaning "falling off," as
leaves from a tree).

The amount of apoptosis that occurs in developing and adult animal
tissues can be astonishing. In the developing vertebrate nervous system,
for example, up to half or more of the nerve cells normally die soon
after they are formed. In a healthy adult human, billions of cells die
in the bone marrow and intestine every hour. It seems remarkably
wasteful for so many cells to die, especially as the vast majority are
perfectly healthy at the time they kill themselves. What purposes does
this massive cell death serve?

In some cases, the answers are clear. Mouse paws, for example, are
sculpted by cell death during embryonic development: they start out as
spadelike structures, and the individual digits separate only as the
cells between them die (Figure 17-35). In many other cases, cell death
helps regulate cell numbers. In the developing nervous system, for
example, cell death adjusts the number of nerve cells to match the
number of target cells that require innervation. In all these cases, the
cells die by apoptosis.

In adult tissues, cell death exactly balances cell division. If this
were not so, the tissue would grow or shrink. If part of the liver is
removed in an adult rat, for example, liver cell proliferation increases
to make up for the loss. Conversely, if a rat is treated with the drug
phenobarbital - which stimulates liver cell division (and thereby liver
enlargement) - and then the phenobarbital treatment is stopped,
apoptosis in the liver greatly increases until the liver has returned to
its original size, usually within a week or so.  Thus, the liver is kept
at a constant size through the regulation of both the cell death and the
cell birth rate.

...

The intracellular machinery responsible for apoptosis seems to be
similar in all animal cells. This machinery depends on a family of
proteases that have a cysteine at their active site and cleave their
target proteins at specific aspartic acids. They are therefore called
*caspases.* Caspases are synthesized in the cell as inactive precursors,
or /procaspases,/ which are usually activated by cleavage at aspartic
acids by other caspases (Figure 17-38A). Once activated, caspases
cleave, and thereby activate other procaspases, resulting in an
amplifying proteolytic cascade (Figure 17-38B). Some of the activated
caspases then cleave other key proteins in the cell. Some cleave the
nuclear lamins, for example, causing the irreversible breakdown of the
nuclear lamina; another cleaves a protein that normally holds a
DNA-degrading enzyme (a DNAse) in an inactive form, freeing the DNAse to
cut up the DNA in the cell nucleus. In this way, the cell dismantles
itself quickly and neatly, and its corpse is rapidly taken up and
digested by another cell.

Activation of the intracellular death pathway, like entry into a new
stage of the cell cycle, is usually triggered in a complete, all-or-none
fashion. The protease cascade is not only destructive and
self-amplifying but also irreversible, so that once a cell reaches a
critical point along the path to destruction, it cannot turn back.

...

In the best understood pathway, mitochondria are induced to release the
electron carrier protein /cytochrome c/ (see Figure 14-26) into the
cytosol, where it binds and activates an adaptor protein called *Apaf-1*
(Figure 17-39B). This mitochondrial pathway of procaspase activation is
recruited in most forms of apoptosis to initiate or to accelerate and
amplify the caspase cascade. DNA damage, for example, as discussed
earlier, can trigger apoptosis. This response usually requires p53,
which can activate the transcription of genes that encode proteins that
promote the release of cytochrome /c/ from mitochondria. These proteins
belong to the Bcl-2 family.
-----

  So it's no coincidence that cancerous cells' mitochondria aren't
"healthy." Cancer thrives by interfering with mechanisms in the
mitochondrion which ordinarily would cause the orderly death and
disintegration of the cell, *but* it does so without interfering with
those cell functions it needs to survive and grow.

Now this is an interesting point I would like to know more about.  I
had the feeling that AA is not used for energy storage in the adipose
tissues.  The shorter Omega-6 version linoleic acid (LA) is used
instead and reflects its dietary intake (this may turn quite dangerous
if you get cancer and start "burning" such LA-rich fat).  Most storage
fat would be normally made from carbohydrates and would be therefore
SFA or MUFA (oleic acid) like the animal lard.  I don't think there is
enough AA in meat to be put into the adipose tissue storage?  Or are
you suggesting that the adipocytes or liver have so robust
desaturation and elongation pathways that a significant amount of
ingested LA is converted into AA for storage?  In my current view most
AA is put into cell and mitochondrial membranes to be used for local
signaling when the cells are mechanically or chemically stressed (e.g.
by nitric oxide or high dose of VitB3).  And it is not only
intracellular matter but the prostaglandins and leukotrienes can
diffuse in tissues some distance (e.g. LTB4 acts as powerful
chemoattractant for the destructive leukocytes).

Also interesting that nothing has been reported about the EFAD effects
on brain (in adults).  No neurodegeneration from AA insufficiency but
rather the other way around.  Either the brain has a very good
mechanism holding on to the "EFA" stores or it doesn't need them.
AFAIK EFAD has only effects on skin and this may not even be related
to AA but LA.

Taka

  (Let's reserve "AA" for "amino acid.")  Nobody would ever have
thought of adding MSG to food if it weren't already found in food.  Some
of that glutamate, at least, goes into muscles and other tissues, and
enzymes, and it spares the energy and niacin required to make it from
alpha-ketoglutarate, a Krebs cycle intermediate.

  Can you point me to more information on both these subjects -- AA in
muscle fibers and DHA in neurons?

  Omega-3 supplements generally contribute small amounts of omega-3s
compared to fatty fish, don't they?  Isn't it likely that humans
consumed much larger amounts of them in other times and places?

  Is it fair to say that most scientists consider the accumulation of
Mead acid in adipose tissue to indicate a pathological condition, but
Ray Peat disagrees, and that you are open-minded towards his position?